Links for Keyword: Parkinsons
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By Ingrid Wickelgren If your hands and arms quiver when you write and do other tasks, you may have a common neurological condition called essential tremor (ET). As many as 7 percent of adults older than 65 suffer from ET, which may also affect the head and voice. In severe cases, it can be disabling. The cause of such shaking has long been mysterious. But researchers are beginning to uncover a biological explanation for the problem: they have found a gene that may contribute to its development as well as a pathological signature of the disorder in the brain. Researchers knew that genetic factors underlie ET, as half or more of the cases run in families. But no one until now had succeeded in nabbing any of the responsible genes. To find such a gene, scientists at deCODE genetics in Iceland compared DNA blueprints from hundreds of tremor patients and thousands of unafflicted residents. In each person’s DNA, researchers looked at 305,624 single-nucleotide polymorphisms (SNPs), sites where the identity of the chemical unit (the pair of molecules that makes up each building block of a strand of DNA) commonly varies among people. Out of that analysis emerged one SNP that consistently differed between the patients and the others. The same chemical unit also turned out to be tied to ET in populations of patients whom the researchers recruited from Germany, Austria and the U.S. The newly fingered SNP lies in a gene for a protein called LINGO1 that is present only in the brain and spinal cord—a distribution consistent with a role in neurological disorders, says neurologist Dietrich Haubenberger of the Medical University of Vienna in Austria, one of the study’s authors. The protein, which straddles the cell membrane, is thought to govern interactions among cells and to thereby influence neuronal integrity as well as function. LINGO1 also has been implicated in multiple sclerosis and Parkinson’s disease, but its precise role in these disorders and in ET is unclear. © 1996-2009 Scientific American Inc.
By DARCY HELLER STERNBERG I can spot Marty in a crowd a block away. He tilts left into the wind, as if he were shouldering the full blast of Hurricane Katrina, his arm gesticulating awkwardly. Once a well-dressed woman asked if I had seen “that man — I think he’s drunk.” I assured her the man was my husband. “He has Parkinson’s,” I told her. We get that a lot — snickers, whispers. Looks that wound. “When people stare,” Marty tells me, “I get nervous and shake that much more.” There are no rules of etiquette for dealing with a person who has a neurological disorder. Some people do stare; others recoil. Fortunately, though, many are genuine and forthcoming in their help. And that is as true here in New York City, supposedly the capital of heartless impatience, as it is anywhere in the country. Marty has to take a combination of seven drugs eight times a day. He bought an expensive pillbox specifically made for Parkinson’s patients; an alarm goes off when it’s time to take a pill. One problem: the container is so difficult to open that when he finally succeeds, the pill is likely to go flying across the room or, worse, into the street. Even when he’s able to grasp the pill and take it, it may not last as long as he would like. “After a few years of taking medication, people with Parkinson’s may begin to experience ‘wearing off’ spells,” Dr. Lawrence I. Golbe, a neurologist at Robert Wood Johnson University Hospital in New Brunswick, N.J., recently wrote in the Parkinson’s Disease Foundation newsletter, adding that for some patients the drugs may be effective for only three hours. Copyright 2009 The New York Times Company
by Jessica Hamzelou Boosting brain waves can make people move in slow motion. This finding is one of the first to show that brain waves directly influence behaviour, and it could lead to new treatments for Parkinson's disease and other disorders that affect movement. Peter Brown and his colleagues at University College London generated a small electrical current in the brains of 14 healthy volunteers using scalp electrodes. The current increased the activity of normal beta waves – a kind of brain wave that is usually active during sustained muscle activities, such as holding a book. Beta activity usually drops before people begin a movement. The participants then carried out a simple task: they moved a spot on a computer screen as quickly as possible using a joystick. When beta wave activity increased, their fastest times slowed by 10 per cent. "This is the first time that beta wave activity has been shown to slow movement," Brown says. Other studies have found that people with Parkinson's disease have greater beta activity. Brown's research suggests this could be linked to the slowing of movement seen in those with the disease. Electrical stimulation deep in the brain is used to treat people with Parkinson's, although how it works is a subject of debate. © Copyright Reed Business Information Ltd
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 10: Biological Rhythms and Sleep
Link ID: 13321 - Posted: 06.24.2010
Peter Aldhous Therapeutic cloning works – in mice, at least. An international team has restored mice with a condition similar to Parkinson's disease back to health, using neurons grown in the lab that were made from their own cloned skin cells. This is the first time that a disease has been successfully treated using cloned cells that had been derived from the recipient animals. "It is the proof of concept," says Lorenz Studer of the Sloan-Kettering Institute in New York, US, who led the research. But he warns that is too early to say whether the technique can be developed into a practical therapy for human patients. Studer's team first gave mice a drug to kill neurons that make the neurotransmitter dopamine. This caused movement problems similar to those seen in people with Parkinson's disease. Then the researchers took biopsies from the tails of these mice and shipped them to Teruhiko Wakayama, a specialist in cloning at the RIKEN Center for Developmental Biology in Kobe, Japan. Wakayama's team transferred the nuclei from skin cells taken from these biopsies into mouse eggs stripped of their chromosomes, to create embryos. The Japanese researchers extracted embryonic stem (ES) cells from these cloned embryos, creating a total 187 ES cell lines from 24 mice. © Copyright Reed Business Information Ltd
Human trials of isradipine (or DynaCirc) – which is prescribed for hypertension and stroke – are now planned. Over time, Parkinson's patients lose a set of brain cells that produce the crucial signalling chemical dopamine – and these cells do not regenerate. Without enough dopamine, people cannot control their body movements and ultimately develop severe neurological problems, including dementia. Scientists have struggled to understand why the dopamine-producing brain cells start dying, but ageing plays a strong role. James Surmeier at Northwestern University in Illinois, US, and colleagues found that in young mice these cells use sodium channels to send signals, but in older mice they rely more on a certain kind of calcium channel. This can prove deadly for a neuron because calcium accumulates inside the cell, eventually triggering a complete breakdown. Surmeier wondered whether he could reverse the switch to calcium channels: "The cells had put their old childhood tools in the closet. The question was, if we stopped them from behaving like adults, would they go into the closet and get them out again?" © Copyright Reed Business Information Ltd
By Michael Day People with Parkinson's disease are three times more likely than non-sufferers to have been troubled by allergic rhinitis – an inflammatory nasal response to pollen or other airborne particles – a new study finds. The results suggest that allergic diseases, such as hay fever, may be linked to brain inflammation that hastens the onset of the neuro-degenerative disorder, say researchers at the Mayo Clinic in Rochester, Minnesota, US. Previous studies have shown that non-steroidal anti-inflammatory drugs, such as ibuprofen, offered some protection against Parkinson's disease. These results prompted clinical neurologist James Bower and colleagues to investigate the links between inflammatory conditions and Parkinson’s disease. They studied 196 people with Parkinson’s disease and 196 others matched for age and gender. A comparison of the two groups revealed that those with Parkinson’s were 2.9 times more likely to have suffered rhinitis earlier in their lives. "People with allergic rhinitis mount an immune response with their allergies, so they may be more likely to mount an immune response in the brain as well, which would produce inflammation," Bower says. © Copyright Reed Business Information Ltd
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 9223 - Posted: 06.24.2010
ST. PAUL, Minn. – People with Parkinson disease can be apathetic without being depressed, and apathy may be a core feature of the disease, according to a study published in the July 11, 2006, issue of Neurology, the scientific journal of the American Academy of Neurology. Apathy is a mental state characterized by a loss of motivation, loss of interest, and loss of effortful behavior. In apathy, the mood is neutral and there is a sense of indifference. In depression, the mood is negative and there is emotional suffering. Because apathy and depression share some of the same symptoms, the disorders can be misdiagnosed. “This study shows that it’s important to screen for both apathy and depression so patients can be treated appropriately,” said study author Lindsey Kirsch-Darrow, MS, of the University of Florida in Gainesville. “It will also be important to educate family members and caregivers about apathy to help them understand that it is a characteristic of Parkinson disease. Apathetic behavior is not something the patient can voluntarily control, and it is not laziness or the patient trying to be difficult – it is a symptom of Parkinson disease.” The study compared 80 people with Parkinson disease to 20 people with dystonia, another movement disorder. The researchers hypothesized that apathy would occur more often in people with Parkinson disease, because the disease affects areas of the brain in the frontal cortex that are involved in non-motor activities, whereas dystonia affects areas mainly involved with movement.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 9162 - Posted: 06.24.2010
RICHLAND, Wash.--Parkinson's, Alzheimer's, Lou Gehrig's disease and other brain disorders are among a growing list of maladies attributed to oxidative stress, the cell damage caused during metabolism when the oxygen in the body assumes ever more chemically reactive forms. But the precise connection between oxidation and neurodegenerative diseases has eluded researchers. Now, a study by the Department of Energy's Pacific Northwest National Laboratory and UCLA's David Geffen School of Medicine reveals that damage is linked to a natural byproduct of oxidation called nitration. "We looked at a healthy brain and found nitration of proteins that are implicated in neurodegenerative disease," said Colette Sacksteder, PNNL scientist and lead author of the study, published in the July issue of the journal Biochemistry (online Wed., June 28). PNNL scientist Wei-Jun Qian was co-lead author. The results are from the most detailed proteomic analysis of a mammalian brain to date – that is, a survey of nearly 8,000 different, detectable proteins in the mouse brain. The research suggests that many neurodegenerative diseases leave a biochemical calling card, or biomarker, that could be used to predict the earliest stages of brain impairment. Many biomedical researchers believe that detecting disease states before symptoms occur is the key to reversing many as-yet-incurable diseases.
CHICAGO – Eleven patients with Parkinson's disease (PD) developed pathological gambling behavior following dopamine agonist therapy, a drug therapy to control movement problems caused by Parkinson's disease, according to a study posted online today which will appear in the September print issue of Archives of Neurology, one of the JAMA/Archives journals. Parkinson's disease, a degenerative disorder marked by the death of the neurons of an area of the brain called the substantia nigra, is primarily treated by drugs that restore or improve brain chemical signaling system dependent on dopamine, according to background information in the article. Brain dopamine, a chemical that helps regulate movement, balance and walking, also plays a central role in the behavioral reward system, reinforcing a myriad of behaviors. It has been implicated in the reward of gambling behavior. M. Leann Dodd, M.D., of the Mayo Clinic, Rochester, Minn., and colleagues, present reports of eleven patients seen and evaluated between 2002 and 2004 in the Mayo movement disorders clinic with Parkinson's disease who had recently developed pathological gambling and review similar cases from the medical literature. Pathological gambling is defined as a failure to resist gambling impulses despite severe personal, family or vocational consequences
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 7628 - Posted: 06.24.2010
A drug that relieves the symptoms of Parkinson’s disease – but was controversially withdrawn over toxicity fears – has now been shown to stimulate growth of the nerve fibres damaged by the disease. When delivered directly to the brain, glial cell-line derived neurotrophic factor (GDNF) had been shown to stimulate regrowth of cells in animal models of Parkinson’s. But this is the first time regrowth has been seen in the human brain, says Steven Gill, a neurosurgeon at Frenchay Hospital, Bristol, UK. Gill was running a trial study where five patients with advanced Parkinson’s disease were fitted with a tiny catheter that delivered GDNF direct to the putamen, part of the basal ganglia in the centre of the brain. In the putamen of Parkinson’s patients the chemical messenger dopamine is lost. The symptoms of Parkinson’s - which include uncontrollable shaking and trembling - were reduced in all five patients. They showed dramatic improvements with respect to their motor skills, verbal memory, facial expressions and motivation. However, Amgen, the company that makes GDNF, withdrew the drug after fears over its toxicity and a second trial of 34 patients was halted. That was despite the fact that the toxicity trials involved testing far higher doses of GDNF on animal models, and that none of the human subjects had showed any ill-effects. © Copyright Reed Business Information Ltd.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 7585 - Posted: 06.24.2010
DALLAS – Researchers at UT Southwestern Medical Center have discovered a mechanism that causes a protein to clump together in brain cells of people with Parkinson's disease, pointing toward a possible treatment for the condition. The protein clumping is part of a "vicious cycle," the researchers said. As the proteins cluster, they inhibit an enzyme that normally breaks them down, leading to the formation of even more masses. "It's a disease involving accumulation of a protein in an aberrant form," said Dr. Philip Thomas, professor of physiology at UT Southwestern and senior author of the study. The research, available online, was published in the June 17 issue of The Journal of Biological Chemistry. The findings have parallels to other diseases in which protein clusters form in and around nerves, such as Huntington's and Alzheimer's disease. The culprit in Parkinson's is the protein alpha-synuclein, which normally appears in a long, folded form in cells. It's known to be linked to the disease because mutations in it cause rare, inherited cases of early-onset Parkinson's. Normally, if a cell becomes stressed, alpha-synuclein unfolds, and an enzyme degrades it completely into harmless bits to prevent the clumping. In Parkinson's patients, however, some of the degrading enzyme malfunctions and creates truncated fragments of alpha-synuclein rather than the harmless bits.
CHICAGO – Deep brain stimulation of two different areas of the brain appears to improve problems with uncontrolled movements (dyskinesia) in patients with Parkinson disease (PD), according to an article in the April issue of Archives of Neurology, one of the JAMA/Archives journals. Deep brain stimulation with electrical impulses delivered to structures deep within the brain is being intensively investigated for the management of advanced Parkinson disease, according to background information in the article. Although a number of studies have shown that stimulation of two different areas of the brain, the globus pallidus interna (GPi) and the subthalmic nucleus (STN), can be achieved safely and effectively, STN has been thought to be the preferred target. At the same time, the authors note, there does seem to be some evidence that the STN is more vulnerable during surgery and that STN patients may have more postoperative problems. Valerie C. Anderson, Ph.D., of the Oregon Health and Science University, Portland, and colleagues compared 23 patients with Parkinson disease and problems with medication-induced uncontrolled movement who were randomly assigned to implantation of deep brain stimulators in either the GPi or the STN areas of the brain. Patients' Parkinson symptoms were evaluated with and without medication using a standard rating scale at three, six and 12 months after surgery.
INDIANAPOLIS – A mutation in a recently discovered Parkinson's disease gene is believed to be the most common genetic cause of inherited forms of the disease, according to a Parkinson Study Group study appearing in The Lancet in January. Researchers say the mutation on the LRRK2 gene is responsible for 5 percent of inherited Parkinson's disease cases. Tatiana Foroud, Ph.D., associate professor of medical and molecular genetics at Indiana University School of Medicine and principal investigator on the multi-site study, said the discovery has a broad implication for genetic screening for the disease. "Our results suggest that the mutation we have studied is the most common cause of Parkinson's disease identified to date," said Dr. Foroud. "While a great deal of work remains to be done, it is clear that any future genetic testing for Parkinson's disease must include studies of the LRRK2 gene." The patients in the Indiana University study who had the mutation had longer disease duration but less severe symptoms when they were participating in the trial. That suggests that the mutation may be associated with slower disease progression, said Dr. Foroud.
PORTLAND, Ore. – A peculiar form of a gene mutation known to increase a person's risk for Parkinson's disease is puzzling doctors about how to counsel patients who have the anomaly. A study by researchers at the Oregon Health & Science University School of Medicine's Parkinson Center of Oregon, the University of Washington School of Medicine and the New York State Department of Health, Wadsworth Center, raises concerns about whether patients testing positive for a single mutation of the parkin gene, rather than the two mutations typically required for developing Parkinson's, can be accurately informed about their risks of developing the disease or passing it on to their children. The study represents "a call for getting more information about the gene," said John "Jay" G. Nutt, M.D., OHSU professor of neurology, and physiology and pharmacology, and Parkinson center director. "What are the clinical implications of finding this gene?" What's alarmed doctors is that in the clinical setting, the single mutation appears to be common: 18 percent of patients with early-onset Parkinson's disease – those diagnosed before age 40 – tested positive for parkin gene mutations, and of that group, 70 percent had only one mutation.
But antidepressant Paxil has no effect on physical symptoms PORTLAND, Ore. – A well-known drug used to treat hyperactive children boosts the potency of another drug that reduces Parkinson's disease symptoms, an Oregon Health & Science University study has found. Scientists at the OHSU Parkinson Center of Oregon found that methylphenidate, known commercially as Ritalin, bolsters the effects of levodopa, a drug converted in the brain to dopamine. Methylphenidate inhibits the reabsorption of dopamine into nerve cells, increasing the neurotransmitter's potency. Parkinson's disease is caused by a deficiency of nerve cells that produce dopamine. A parallel study by Parkinson center researchers found that paroxetine, a popular antidepressant best known under the brand name Paxil, doesn't augment the effects of levodopa and has little benefit in reducing physical symptoms of Parkinson's disease.
ST. PAUL, MN – People with high levels of iron in their diet are more likely to develop Parkinson's disease, according to a study in the June 10 issue of Neurology, the scientific journal of the American Academy of Neurology. People with both high levels of iron and manganese were nearly two times more likely to develop the disease than those with the lowest levels of the minerals in their diets. The study compared 250 people who were newly diagnosed with Parkinson's to 388 people without the disease. Interviews were conducted to determine how often participants ate certain foods during their adult life. Those who had the highest level of iron in their diets – in the top 25 percent – were 1.7 times more likely to be Parkinson's patients than those in the lowest 25 percent of iron intake. Those whose level of both iron and manganese was higher than average were 1.9 times more likely to be Parkinson's patients than those with lower than average intake of the minerals.
Findings suggest how tiny jolts can steady tremor sufferers By ALEXANDRA WITZE / The Dallas Morning News ORLANDO, Fla. – Everybody likes to stimulate their brains, usually to make themselves feel smarter. But for some people, it's a medical necessity. People who suffer from Parkinson's or other tremor-related diseases sometimes benefit from deep brain stimulation – a surgery in which doctors implant a small device that sends an electrical signal to a specific part of the brain. Just as a pacemaker uses electricity to regulate an erratic heartbeat, deep brain stimulation uses electricity to pace the firing of nerve cells, or neurons, that control movement. Used with or instead of medication, the surgery often lets patients regain control over involuntary jerks like those experienced during Parkinson's. But nobody knows why. ©2002 Belo Interactive
First-ever clinical trials using gene therapy for Parkinson's disease anticipated to begin by end of year – Auckland, New Zealand and New York, NY: In a study published today in the journal Science, scientists from the University of Auckland and Weill Cornell Medical College reported on the effectiveness of a new gene therapy approach to Parkinson's Disease, and the potential for this therapy to affect the overall progression of the disease itself. Based on this study and other data, the U.S. Food and Drug Administration (FDA) has given its approval to begin testing this therapy in a small Phase I clinical trial. This will be the first time in the world that gene therapy will be used in patients with Parkinson's Disease. The Science publication is authored by lead investigator, Dr. Matthew J. During, Professor of Molecular Medicine at the University of Auckland, first author Dr. Jia Luo, and co-investigator Dr. Michael G. Kaplitt, Director of Stereotactic and Functional Neurosurgery and Asst. Professor at Weill Cornell Medical College. Dr. During and Dr. Kaplitt are also co-principal investigators on the upcoming clinical trial of this therapy. "We are using gene therapy to "re-set" a specific group of cells that have become overactive in an affected part of the brain, causing the impaired movement and other symptoms associated with Parkinson's Disease," said Dr. During. "We are very encouraged that in addition to the affect this therapy has on quieting symptoms, we present evidence that suggests it may arrest or delay disease progression."
GAINESVILLE, Fla.---Scientists report this week they have demonstrated that the injection of two corrective genes into a specific brain region generated significant restoration of normal limb movement in rats with a chemical-induced form of Parkinson’s disease. The findings – by a team of researchers from the University of Florida in Gainesville and Lund University in Lund, Sweden – are published in the current online version of the journal of the Proceedings of the National Academy of Sciences. Neuroscientists Anders Bjorklund of Sweden and Ronald Mandel with UF said the strategy that proved effective in the rodents is not a cure for Parkinson’s disease, but is expected to lead to a better method for delaying and controlling symptoms of the progressively disabling condition. About 1 million Americans are affected by Parkinson’s disease, which occurs most often between the ages of 65 and 90. "We found that the simultaneous delivery of two selected genes, coupled with a powerful gene-activating agent, works like a pump to prime the production of L-dopa, which is then converted into dopamine by appropriate nerve cells in the brain," said Mandel, a professor of neuroscience with UF’s Evelyn F. and William L. McKnight Brain Institute and the UF Genetics Institute. Dopamine is a neurotransmitter chemical that plays a lead role in coordinating limb movements.
NASHVILLE, Tenn., – It was a warm summer night that Tuesday – a night not unlike many others he had spent working in the lab – when Richard Nass, Ph.D. walked down the empty hallway and entered a small, darkened room. Settling himself onto a stool, he placed a shallow dish on the stage of the microscope before him and peered through the eyepieces. What he saw there – or, rather, didn’t see – took him aback. Nass saw the host of wriggling, transparent worms that he expected, but missing was the distinctive green glow that should have lit up the bodies of the worms like neon. "I almost couldn’t believe it," he said, shaking his head. The loss of green fluorescence that Nass observed in his worms told him that their dopamine neurons, which had been genetically altered to fluoresce green, had been destroyed by exposure to a chemical, 6-hydroxydopamine (6-OHDA). The results of the study, published this week in the journal Proceedings of the National Academy of Sciences, suggest that this tiny roundworm, named C.elegans, can serve as a powerful model for studying the molecular mechanisms underlying degeneration of dopamine neurons in the brains of patients with Parkinson’s disease (PD).